Continuous 12-lead ECG Monitoring Research Articles

Exercise-induced ventricular arrythmia in asymptomatic patients with Mitral Valve Prolapse

Abstract Introduction Mitral Valve Prolapse (MVP) is associated with complex ventricular arrythmia (VA) and sudden cardiac death but risk stratification remains unclear. Exercise induces an hyperadrenergic state and could trigger VA, however, data on exercise-induced VA (EIVA) in MVP patients are scarce. Objective To describe EIVA prevalence, origin, characteristics and associated features in MVP patients. Methods In this observational prospective study, 64 MVP asymptomatic patients (58±14 years, 41 men) with mild to severe mitral regurgitation (MR) and without left ventricular (LV) dysfunction, underwent echocardiography and symptom-limited exercise testing. Continuous 12-lead ECG monitoring was performed throughout testing. Severe EIVA was defined as ventricular triplets, sustained or non-sustained ventricular tachycardia (NSVT) or ventricular fibrillation. Results All patients exercised at maximal intensity until exhaustion. EIVA was observed in 54 (84%) subjects including 12 (19%) patients with severe EIVA (7 triplets, 5 NSVT). Severe EIVA originated mainly from the mitral apparatus (all but one) and occurred at high exercise intensity (median 90% of predicted workload) or during early recovery phase. Compared to the rest of the cohort the patients with severe EIVA had similar resting ECG characteristics, similar LV dimension and function, similar degree of MR and mitral apparatus morphology. Finally, severe EIVA was not associated with an alteration of exercise tolerance. Conclusion Exercise frequently unmasks ventricular arrythmia in patients with MVP. EIVA appears not linked to MVP features nor to exercise tolerance and seems to provide additional phenotyping information that could be linked to prognosis. Funding Acknowledgement Type of funding sources: None.

Effect of beta-blockade on quantitative microvolt T-wave alternans in 24-hour continuous 12-lead ECG recordings in patients with long QT syndrome.

The aim of study was to investigate effects of beta-blockade on microvolt T-wave alternans (TWA), a precursor of lethal arrhythmia, in patients with long QT syndrome (LQTS). Eleven consecutive LQTS patients, types 1 (n=6), 3 (n=2), and "non-1, non-2, non-3" (n=3) were enrolled. All patients underwent 24-hr continuous 12-lead ECG monitoring before and after initiation of beta-blockade therapy. TWA was measured using the modified moving average method. Seven (63.6%) of the 11 patients studied were symptomatic, with history of cardiac arrest or documented Torsade de Pointes (TdP) in 4 and syncope in three patients. After a median follow-up of 34months, beta-blockade reduced the number of symptomatic patients to 1 with TdP (p<0.02), in whom TdP frequency decreased from 25 events/60months (0.42 event/month) to seven events/69months (0.1 event/month). In association with this reduction in symptoms, peak TWA decreased by 47% in the cohort after a median of eight months of beta-blockade therapy [from 95 (74-130) to 50 (39.5-64.5) µV, p=0.01]. All patients exhibited TWA ≥42µV before beta-blockade therapy, which eliminated these episodes in four patients. Daily frequency of TWA ≥42µV episodes decreased by 87% [from 15 (6-26) to 2 (0-5) episodes/day, p=0.009]. This study is limited by the small sample size and is mainly hypothesis generating. TWA monitoring deserves further evaluation as a risk marker and a guide to therapy in LQTS patients in future large-scale studies.

White blood cell count and new-onset atrial fibrillation after cardiac surgery

BackgroundPostoperative new-onset atrial fibrillation (PNAF) is the most common complication following cardiac surgery. The inflammatory response, as a potential underlying mechanism, has been extensively studied. In small studies, the white blood cell count (WBC) has been shown to be the only consistent inflammatory marker associated with PNAF. This study aimed to determine the association between perioperative WBC response and PNAF in a larger study cohort. MethodsPatients ≥18years, undergoing elective cardiac surgery with a preoperative sinus rhythm were included. WBC was routinely measured preoperatively, and daily during the first four postoperative days. Main outcomes were the difference between peak postoperative WBC and neutrophil/lymphocyte ratio (N/L ratio) and preoperative WBC and N/L ratio (ΔWBC and ΔN/L ratio respectively). Development of PNAF was evaluated in all patients with continuous 12-lead ECG monitoring. Results657 patients were included and 277 (42%) developed PNAF. Univariable analyses showed a statistically significant relationship between ΔWBC (P=0.030) and ΔN/L ratio (P=0.002), and PNAF. In multivariable analysis no significant relationship was found between ΔWBC (OR: 1.14 per 1×109/L increase; 95% CI: 0.65–2.03; P=0.645), ΔN/L ratio (OR: 1.65 per 1×109/L increase; 95% CI: 0.94–2.90; P=0.089), and PNAF. Increasing age (OR: 1.08 per year; 95% CI: 1.01–1.16; P=0.022) and (additional) valve surgery (versus CABG) (OR: 4.96; 95% CI: 2.07–6.91; P≤0.001) were associated with PNAF. ConclusionsThe perioperative WBC response and its components were not associated with the development of PNAF.

Determination Of IANT Via Heart Rate Variability In Overweight And Obese Subjects

Numerous studies reported that the heart rate variability (HRV) may be used to determine the aerobic-anaerobic thresholds (IANT) in healthy trained participants (Flöter et al. 2012; Karapetian et aI. 2008). PURPOSE: The aim of this study was to assess if the IANT may also be determined in overweight and obese subjects utilizing the non-linear response of HRV. METHODS: 28 overweight and obese participants (age: 38.5 + 13.1 yrs; Wt: 96.4 + 16.7 kg; BMI: 30.9 + 4.4 kg-1.m2; %body fat: 29.2 + 4.3; waist circumference: 107.8 + 10.9 cm) completed a two stage incremental test on cycle ergometer (Braumann et al. 1993) followed by continuous performance test to determine and validate the lactate thresholds and IANT as described by Heck et al. 1985. The examination of individual HRV variables and associated HRV thresholds were determined via continuous 12-lead ECG monitoring and recordings (Flöter et al. 2012). The agreement of resulting power output thresholds expressed in Watts (W) in the region of IANT and those determined from HRV recordings were ascertained via Bland-Altman plots and correlation analysis. RESULTS: The calculated thresholds generated from HRV recordings were above those performed in IANT (W: 126 + 30.7; utilizing the Pointcare Chart variability, SD1 of 144.8 + 32.9 = standard deviation of the short-term RR interval variability of transverse axis; SD2 of 146.1 + 30.5 = standard deviation of the long-term RR interval variability of longitudinal axis; SD1/SD2 ratio of 145.2 + 27.8; SD1/HR ratio of 144.4 + 32.2). The results revealed agreements in IANT determination that were confirmed via Bland-Altman Plots as well as significant correlation coefficients generated from the cycle ergometer power output (SD1 = 0.69; SD2 = 0.61; SD1/SD2 = 0.66; SD1/HR = 0.68). CONCLUSION: The results of this study yielded moderate to strong associations between HRV threshold data and results determined via IANT power output on cycle ergometer. In our overweight and obese participants, the response in HRV variability was present and possible only during the short-term analysis.

Diagnostic performance of treadmill exercise cardiac magnetic resonance: the prospective, multicenter EXACT trial

Methods Patients clinically referred for treadmill stress SPECT for the evaluation of known or suspected CAD were prospectively enrolled across 4 centers. After rest Tc99m SPECT imaging, patients underwent resting cine CMR. In-room stress was then performed using an MR-compatible treadmill with continuous 12-lead ECG monitoring and the Bruce exercise protocol. At peak stress, Tc99m was injected and patients were rapidly returned to their prior position in the magnet for real-time, free-breathing post-exercise cine and perfusion CMR. Following recovery monitoring with the table brought outside of the magnet bore, recovery cine and rest perfusion followed by late gadolinium enhancement acquisitions concluded the CMR portion of the exam. Stress SPECT images were then acquired in the adjacent nuclear laboratory. Patients not referred for invasive coronary angiography (ICA) within 2 weeks of stress imaging underwent coronary angiography with computed tomography (CTA). Diagnostic accuracy and prognostic value of treadmill stress CMR vs. SPECT were evaluated.

Coronary microvascular spasm triggers transient ischemic left ventricular diastolic abnormalities in patients with chest pain and angiographically normal coronary arteries

AimsImpaired coronary microvascular dilatory function can lead to exercise induced myocardial ischemia and angina pectoris even in patients without significant (>50%) obstructive coronary atherosclerosis (APWOCA). Diffuse distal vessel epicardial spasm and microvascular spasm have been also proposed as a plausible explanation for angina at rest in these patients. However, objective systematic evidence for the latter i.e. echocardiographic wall motion abnormalities during angina, is lacking at present. Coronary epicardial and microvascular spasm can be triggered in susceptible patients by the administration of intracoronary acetylcholine (Ach). We sought to assess whether Ach induced diffuse distal epicardial coronary artery spasm (≥75% diameter reduction) and coronary microvascular spasm can cause transient ischemic left ventricular dysfunction, as assessed by echocardiography. Methods50 patients (19 men aged 60.5 ± 8.9 years) with stable APWOCA were assessed for coronary spasm and myocardial ischemia with intracoronary Ach infusion, 2D transthoracic echocardiography (before and during Ach testing), continuous 12-lead ECG monitoring, and ultrasensitive cardiac troponin (US-cTn) measurement before and within 4 h after Ach testing. Results14 patients (28%) had a “negative” Ach test, 14 (28%) developed coronary microvascular spasm and 17 (34%) had diffuse distal epicardial spasm. In 5 patients (10%) the test was inconclusive. Echocardiographic variables including deceleration time, EF slope and E/A, as well as ultrasensitive-cTn concentrations were abnormal during Ach induced ischemic ECG changes. Conclusions: We have, for the first time, demonstrated that Ach induced coronary microvascular spasm is associated with echocardiographic changes and ultrasensitive-cTn elevations, indicative of myocardial ischemia.

T wave alternans in experimental myocardial infarction: Time course and predictive value for the assessment of myocardial damage

BackgroundT-wave alternans (TWA) is associated with prognosis after myocardial infarction (MI), however its link to the extent of ischemic injury has not been clarified. We analyzed the course of TWA and its relation to myocardial damage in experimental myocardial infarction. MethodsIn 21 pigs, infarction was induced by 40-minute long balloon inflation in LAD under continuous 12-lead ECG monitoring. TWA was assessed in a 32-beat sliding window, using periodic component analysis and the Laplacian Likelihood Ratio method. Myocardium at risk (MaR) and infarct size (IS) were evaluated by SPECT and magnetic resonance imaging respectively. ResultsTWA appeared at 7.2±4.5minutes of occlusion, reached its maximum at 12.7±6.3 and lasted until 26.5±9.2minutes. The maximal level of TWA was associated with both MaR (r=0.499, p=0.035) and IS (r=0.65, p=0.004). ConclusionTWA magnitude is associated with both MaR and IS in experiment, which encourages further studies in clinical settings.

Genotype- and Mutation Site–Specific QT Adaptation During Exercise, Recovery, and Postural Changes in Children With Long-QT Syndrome

Exercise stress testing has shown diagnostic utility in adult patients with long-QT syndrome (LQTS); however, the QT interval adaptation in response to exercise in pediatric patients with LQTS has received little attention. One-hundred fifty-eight patients were divided into 3 groups: Those with LQTS type 1 (LQT1) or LQTS type 2 (LQT2) and normal control subjects without cardiovascular disease. Each patient underwent a uniform exercise protocol with a cycle ergometer followed by a 9-minute recovery phase with continuous 12-lead ECG monitoring. Each patient underwent a baseline ECG while resting in the supine position and in a standstill position during continuous ECG recording to determine changes in the QT and RR intervals. Fifty patients were gene-positive for LQTS (n=29 for LQT1 and n=21 for LQT2), and the control group consisted of 108 patients. QT interval adaptation was abnormal in the LQT1 patients compared with LQT2 and control patients (P<0.001). A corrected QT interval (QTc) >460 ms in the late recovery phase at 7 minutes predicted LQT1 or LQT2 versus control subjects with 96% specificity, 86% sensitivity, and a 91% positive predictive value. A recovery ΔQTc((7 min-1 min)) >30 ms predicted LQT2 versus LQT1 with 75% sensitivity, 82% specificity, and a 75% positive predictive value. The postural ΔQT was significantly different between LQTS and control groups (P=0.005). Genotype-specific changes in repolarization response to exercise and recovery exist in the pediatric population and are of diagnostic utility in LQTS. An extended recovery phase is preferable to assess the repolarization response after exercise in the pediatric population.

Serial snapshot electrocardiograms and continuous 12-lead ST-segment electrocardiographic monitoring for the prediction of intravenous thrombolysis outcome in patients with ST-segment elevation myocardial infarction

We compared the effectiveness of serial snapshot ECGs (S-ECG) and continuous 12-lead ST-segment ECG monitoring (C-ECG) for the prediction of intravenous thrombolysis outcome in 786 patients with ST-segment elevation myocardial infarction. It was found that S-ECG overestimated thrombolysis success over C-ECG by 7.1%. By 1-year patients who were diagnosed as having successful thrombolysis by S-ECG but not by C-ECG were at significantly higher risk of 1-year cardiac death than those who were classified as having successful thrombolysis by both ECG methods, and were at similar risk of 1-year cardiac death than those who were classified as having failed thrombolysis by both ECG methods.

Automatic Extraction of ECG Strips from Continuous 12‐lead Holter Recordings for QT Analysis at Prescheduled versus Optimized Time Points

Continuous 12-lead ECG monitoring (Holter) in early-phase pharmaceutical studies is today widely used as an ideal platform to extract discrete ECGs for analysis. The extraction process is typically performed manually by trained readers using commercial Holter processing systems. Antares, a novel method for automatic 12-lead extraction from continuous Holter recordings applying minimal noise criteria and heart-rate stability conditions is presented. A set of 12-lead Holter recordings from healthy subjects administered with sotalol is used to compare ECG extractions at fixed time points with ECG extractions generated by Antares optimizing noise and heart rate inside 5 minute windows centered around each expected time point of interest. Global, low- and high-frequency noise content of extracted ECGs was significantly reduced via optimized approach by Antares. Heart rate was also slightly reduced (from 69 +/- 13 to 64 +/- 13 bpm, P < 0.05). Similarly, the corrected QT interval from optimized extractions was significantly reduced (QTcB from 414 +/- 32 to 402 +/- 30 ms, P < 0.05). Using only baseline data, and after adjusting for intersubject variability, the standard deviation (SD) of QT intervals was highly reduced with optimized extraction (SD of QTcF from 11 +/- 8 to 7 +/- 2 ms, P < 0.05). Extraction of discrete 12-lead ECG strips from continuous Holter generates less noisy and more stable ECGs leading to more robust QTc data, thereby potentially facilitating the assessment of ECG effects on clinical trials.

Silent Myocardial Ischemia

Silent myocardial ischemia is defined as objective documentation of myocardial ischemia in the absence of angina or anginal equivalents. Since its original description in the 1970s, it has undergone intensive investigation, and its clinical significance is now well established. This review will serve as an update on the pathophysiology, detection, prevalence, prognosis, and treatment of silent ischemia in both asymptomatic patients and those with angina, whether stable or unstable. ### Pain Studies No discussion of silent ischemia is complete without consideration of the cardiac pain mechanism. Although much has been learned about this subject, much is still uncertain. The afferent fibers that run in the cardiac sympathetic nerves are usually thought of as the essential pathway for the transmission of cardiac pain (Figure 1). The atria and ventricles are abundantly supplied with sympathetic sensory innervation; from the heart, the sensory nerve endings connect to afferent fibers in cardiac nerve bundles, which in turn connect to the upper 5 thoracic sympathetic ganglia and the upper 5 thoracic dorsal roots of the spinal cord. Within the spinal cord, impulses mediated by this sympathetic afferent route probably converge with impulses from somatic thoracic structures onto the same ascending spinal neurons. This would be the basis for cardiac pain referred to the chest, wall, arm, back etc. In addition to this “convergence-projection theory,” the contribution of vagal afferent fibers must be acknowledged for an explanation of cardiac pain referred to the jaw and neck. How these vagal fibers are activated remains unclear. Furthermore, somatic localization of ischemic pain cannot predict the site of myocardial ischemia (anterior, inferior, or lateral) from one patient to the next. Figure 1. Mechanisms of cardiac pain. From Droste and Roskamm (used with permission).4 The actual “trigger” that stimulates the sensory nerve endings remains elusive. If a chemical pain stimulus is involved, …

Continuous 12-Lead ECG Monitoring in an ED Chest Pain Unit

The protocols used in chest pain units (CPUs) to rule out acute MI and to diagnose acute coronary syndromes (ACSs) are not standardized. In this

Continuous 12-lead electrocardiographic monitoring in an emergency department chest pain unit: An assessment of potential clinical effect

Study objectives: Continuous 12-lead serial ECG monitoring has been proposed to assist in the evaluation of patients with acute coronary syndrome and nondiagnostic ECG in an emergency department chest pain unit. However, the ability of serial ECG to detect acute coronary syndrome and its benefit in addition to a standard protocol has not been established. We evaluate the ability of continuous 12-lead ECG to detect acute coronary syndrome, assess the incremental benefit of the serial ECG in association with a set protocol in an ED chest pain unit, and evaluate whether serial ECG changes could be considered as prognostic factors. Methods: Patients who met Agency for Health Care Policy and Research guidelines for intermediate risk for short-term cardiovascular event unstable angina were prospectively studied in the chest pain unit. Patients were monitored with the Mortara Instruments ELI 100 STM continuous 12-lead ECG system with ST-segment analysis. ST-segment changes of greater than 100 μV in 2 or more contiguous leads or greater than 200 μV in 1 lead were considered positive. Data were compared with serial serum cardiac markers, cardiac function study results, angiographic results, and 30-day outcome results. Results: One hundred nineteen patients had serial ECG applied. The median duration of monitoring was 4.2 hours. Forty patients were given a diagnosis of acute coronary syndrome. Chest pain unit protocol detected 52 patients, and 23 were given a diagnosis of acute coronary syndrome (sensitivity 58%; specificity 63%). Sixteen patients had ST-segment changes of greater than 100 μV or greater than 200 μV, and 9 were given a diagnosis of acute coronary syndrome. The addition of the serial ECG to the chest pain unit protocol increased the sensitivity to 65% and decreased the specificity to 58%. Two patients with ST-segment changes but none without ST-segment changes had an adverse cardiac event, yielding a sensitivity of 100% and a specificity of 88%. Conclusion: Serial ECG is of limited value in the diagnostic evaluation of intermediate-risk patients managed in the chest pain unit with a standard protocol. However, when ST-segment changes are present, they indicate an increased likelihood for an adverse cardiac event. [Ann Emerg Med. 2003;41:342-351.]

A rapid protocol to identify and exclude acute myocardial infarction: Continuous 12-lead ECG monitoring with 2-hour delta CK-MB

A prospective observational study was performed in 706 chest pain patients who underwent our chest pain evaluation protocol which consists of continuous 12-lead ST-segment monitoring with automated serial ECG (SECG) and a 2-hour delta (Δ) CK-MB level determination before ED physician making final disposition decision to determine the incremental value of our 2-hour protocol for identifying myocardial infarction (MI) as compared with the initial ECG in combination with a baseline CK-MB. The initial ECG was obtained on presentation and considered positive if it revealed injury or ischemia. SECGs were obtained at least every 10 minutes and considered positive if it revealed new injury or ischemia. The baseline CK-MB value was considered positive if it was ≥12 ng/mL and index ≥4%. ΔCK-MB was defined as a difference between the 2 hour and baseline CK-MB and was considered positive if the value was ≥+1.5 ng/mL. MI was defined as acute myocardial infarction (AMI) or recent AMI (ie, AMI patients presenting on falling curve of CK-MB). The incremental value of the 2 hour protocol (ie, SECG in conjunction with ΔCK-MB) was more sensitive for identification of MI than the baseline protocol (ie, initial ECG in conjunction with the baseline CK-MB) (94.0% versus 55.4%; P < .0001) and reliably both identified (+LR = 14.6) and excluded MI (−LR = 0.06). SECG monitoring in conjunction with the 2 hour ΔCK-MB allows for early identification and exclusion of MI, and can assist the ED physician in making appropriate treatment and disposition decisions. (Am J Emerg Med 2000;18:698-702.

Incidence and clinical relevance of the occurrence of bundle-branch block in patients treated with thrombolytic therapy.

Whether thrombolytic therapy alters the incidence and clinical outcome of bundle-branch block is unclear. We examined the occurrence of new-onset bundle-branch block, both transient and persistent, in 681 patients with acute myocardial infarction enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction 9 and Global Utilization of Streptokinase and t-PA for Occluded Arteries 1 protocols. Each patient underwent continuous 12-lead ECG monitoring for 36 to 72 hours with the Mortara ST monitoring system. Bundle-branch block was characterized as right, left, alternating, transient, or persistent. The overall incidence of bundle-branch block was 23.6% (n = 161), with transient block in 18.4% (n = 125) and persistent block in 5.3% (n = 36). Right bundle-branch block was found in 13% (n = 89) of the population; left bundle-branch block was found in 7% (n = 48). Alternating bundle-branch block was seen in 3.5% (n = 24) of patients. Left anterior descending artery infarcts accounted for most bundles (54%, n = 79). Patients with bundle-branch block had lower ejection fractions, higher peak creatine phosphokinase levels (P < .0001), and more diseased vessels (P < .019). Mortality rates in patients with and without bundle-branch block were 8.7% and 3.5%, respectively (P < .007). A higher mortality rate was observed in the presence of persistent (19.4%) versus transient (5.6%) or no (3.5%) bundle-branch block (P < .001). Thrombolytic therapy reduces the overall mortality rate associated with persistent bundle-branch block. However, persistent bundle-branch block remains predictive of a higher mortality rate than either transient or no bundle-branch block. Continuous 12-lead ECG monitoring provides an accurate characterization of the incidence and type of conduction disturbances after acute myocardial infarction.

Relation Between Ischemia Time, Infarct Size, and Left Ventricular Function in Humans

Experimental studies indicate that duration of ischemia is a major determinant of myocardial infarct size, but only limited information is available about the relation between ischemia time and infarct size in individual patients. This prospective study sought to document the role of ischemia time as a determinant of infarct size in humans. We studied 61 patients (50 men, 11 women) 57 +/- 11 years old admitted with a first infarct (31 anterior, 30 inferior) who underwent continuous 12-lead ECG monitoring to document ischemia time. Infarct size (32-point QRS score on day 7) and changes in regional myocardial wall motion (echocardiography) during the following month were related to ischemia time. Among patients with < 3 hours of ischemia (n = 16), mean infarct size on day 7 was 21 +/- 13% of potential infarct size; in patients with 3 to 6 hours of ischemia (n = 23), infarct size was 38 +/- 18% of potential (P < .05 versus 0 to 3 hours of ischemia); and in patients with 6 to 9 hours of ischemia (n = 10), infarct size was 66 +/- 14% of potential (P < .05 versus 3 to 6 hours). In contrast, the 12 patients with an ischemia time > 9 hours had a final infarct size of 77 +/- 10% of potential (P < .01 versus 3 to 6 hours). Multivariate regression identified size of risk region, duration of ischemia, and degree of initial ST-segment elevation as independent predictors of infarct size, of which the most important variable was ischemia time. The regression models accurately predicted both individual absolute infarct size (R2 = .83) and individual infarct/risk ratio (R2 = .74). Patients with < 6 hours of ischemia exhibited significant recovery of myocardial wall motion by day 7 (wall motion score, 2.1 +/- 1.4 versus 5.7 +/- 3.2 on day 1, P < .01). Patients with 6 to 9 hours of ischemia had some recovery by 1 month (score, 6.3 +/- 4.4 versus 10.9 +/- 3.8 on day 1, P < .01), but patients with > 9 hours of ischemia had little recovery of wall motion by 1 month (score, 10.3 +/- 4.5 versus 12.8 +/- 3.1 on day 1, P < .05). Measurement of ischemia time allows improved prediction of infarct size in humans. Significant myocardial salvage and functional recovery may be achieved by reperfusion up to 9 hours after coronary occlusion. Continuous ST-segment monitoring should be used to measure ischemia time and guide interventions to reperfuse the infarct artery.

ECG Diagnosis of Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block in Patients Undergoing Continuous ECG Monitoring

It is common knowledge that the ECG diagnosis of completed myocardial infarction in the presence of left bundle-branch block (LBBB) is extremely difficult and often impossible. More than 50 rules have been proposed as criteria for interpreting Q-wave equivalents superimposed on the QRS complex in the presence of LBBB. However, because of misinterpretation of the available literature, physicians frequently recommend that patients with chest pain in the presence of LBBB receive thrombolytic therapy or urgent coronary arteriography on the basis of the assumption that acute injury and ischemia cannot be interpreted in the presence of LBBB. Unfortunately, many physicians fail to realize that although completed infarction is difficult to confirm in the presence of LBBB, ongoing ischemia and injury can be detected in the presence of LBBB and may be seen as often as they are in the presence of normal cardiac conduction. A deflection of the J point (and ST segment) in the direction of the major QRS complex or an elevation of the ST segment of more than 7 to 8 mm opposite the direction of the major QRS complex has been demonstrated to have a sensitivity of more than 50% in detecting acute injury, with a specificity of more than 90%. During the first half of an ongoing prospective study of the use of continuous 12-lead ECG monitoring in the emergency department, we encountered five patients with final diagnoses of acute myocardial infarction in the presence of LBBB who demonstrated significant ECG changes while undergoing continuous ST-segment monitoring with frequent serial ECGs. The five different locations of the infarcts in these five patients were posterior, posterolateral, inferior, anterior, and anterolateral. We present these patients' cases to demonstrate the ECG characteristics of acute injury in the presence of LBBB. [Fesmire FM: ECG diagnosis of acute myocardial infarction in the presence of left bundle-branch block in patients undergoing continuous ECG monitoring. Ann Emerg Med July 1995;26:69-82.]